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The all-or-nothing spikes elicited by antidromic, afferent, or direct electrical stimulation of a cortical area treated with mescaline or strychnine were studied. These potentials are most probably originated in nonsynaptic dentritic membranes and their changes in amplitude and latency can be an index of the excitability of these structures. Several factors are considered as sources of error when measurements of such parameters are made to follow their changes in different experimental conditions. When these sources of error can be eliminated, the frequency, amplitude and latency of those spikes can be taken as an index of the variations in cortical excitability under some physiological conditions. Another use of these giant potentials can be for the study of humoral and pharmacological agents.

The sensitivity of some electrocortical potentials of rats to topically applied tetrodotoxin (TTX), manganese, lanthanum, calcium, mescaline and strychnine was followed from the age of 6 to 20 days and compared with that of adult animals. Sensitivity to TTX was relatively greater in the younger rats. In contrast, the blocking effect of Mn2+ or La3+ was small initially but increased with age. Similarly, the ability of mescaline or strychnine to give rise to giant spikes (dendritic action potentials) increased with maturation of the brain cortex. Finally, an increase in external calcium concentration depressed cortical potentials in the younger animals and had the usual increase of the mescaline or strychnine spikes in the older rats. It is concluded that the formation of calcium channels in dendritic membranes is part of the maturation process of cortical neurons and possibly related to the learning mechanisms. The depressant action of high external calcium during the first days of life was ascribed to an unspecific reduction in membrane permeability.

A depressant reaction of the electrocortical activity of the brain cortex is described. The changes consist in decrease in the amplitude and frequency of the basal waves of the electrocorticogram together with the appearance of slow waves similar to those of the sleep state. The results are more clear upon the dendritic action potentials induced by the topical application of strychnine or mescaline. They include a rise in the threshold to the electrical stimulation applied to elicit these potentials together with a lengthening of their latencies. The depressant effects were obtained by low threshold vagal, carotid sinus, low threshold sciatic and tactile afferent stimulation. Similar depressant effects were produced by serotonin (5-HT) topically applied. The effects of afferent stimulation were reduced in magnitude by an intracisternal injection of 5,6-dihydroxytryptamine. A serotonergic mechanism acting in a diffuse, humoral, way is postulated. The methodological importance of studying the strychnine or mescaline spikes is emphasized.

By using the mescaline or the strychnine spikes as indicators of electrocortical activity it was found that they are increased in size by some catecholamines topically applied. These spikes showed late and long-lasting changes after somatic, as well as after autonomic afferent stimulation. The latter induced by cyanide, light asphyxia, intravenous injections of adrenaline or noradrenaline, and after a small dose of 6-hydroxydopamine. After a dose of this last substance, high enough to deplete the catecholamines of the brain, the late increase in amplitude of the cortical potentials observed following afferent stimulation disappeared leaving a long lasting reduction in that amplitude. The hypothesis is presented that the noradrenaline liberated by the adrenergic nerve fibers reaching the upper layers of the cortex acts on the nonsynaptic dendritic membranes modulating their activity in a humoral-like way. The pattern of this facilitating effect has a different temporal course and is longer lasting than that which is to be expectec only by the arrival of impulses at the cortex during the persistence of the neuronal activation induced by the information input to the CNS.